[Relationship between Helicobacter pylori infection and expression of connexin (Cx) 32 and Cx43 genes in gastric cancer and gastric precancerous lesions].
OBJECTIVE
To investigate the expression of connexin (Cx)32 and Cx43 genes in gastric cancer and precancerous lesion, and to investigate the relation between the changes of expression of Cx32 and Cx43 genes and Helicobacter pylori (Hp) infection.


METHODS
Gastroscopy and biopsy of gastric mucosa were conducted on 33 patients with chronic superficial gastritis (CSG), 88 with precancerous lesion, and 70 with gastric cancer. Hp was detected by rapid urease test, basic fuchsin staining, and 14C-urea breath test. The CagA gene of Hp was determined by PCR. SABC immunohistochemical method was used to detect the expression of Cx32 and Cx43 genes in gastric mucosa biopsy specimens.


RESULTS
The positive expression rates of Cx32 and Cx43 genes were 15.7% and 32.9% respectively in the gastric cancer patients, 51.1% and 54.5% in the patients with precancerous lesion, and 100.0% and 93.9% in the CSG patients. The positive Cx32 and Cx43 expression rates of the gastric cancer and precancerous lesion patients were significantly lower than those of the CSG patients (all P < 0.05). The positive Cx32 expression rate of the gastric cancer patients with Hp infection was 16.7%, not significantly different from that of the gastric cancer patients without Hp infection (13.6%). The positive Cx43 expression rate of the gastric cancer patients with Hp infection was 25%, significantly lower than that of the gastric cancer patients without Hp infection (50%, P = 0.039). The positive Cx32 and Cx43 expression rates and expression intensity of the precancerous lesion patients with Hp infection were all significantly lower than those of the precancerous lesion patients without Hp infection (all P < 0.05). The positive Cx43 expression rate of the gastric cancer patients with CagA+ Hp infection was 17.9%, significantly lower than that of the CagA- Hp group (55.6%, P = 0.027), however, the positive Cx32 expression rate of the gastric cancer patients with CagA+ Hp infection was 12.8%, not significantly different from that of the gastric cancer patients with CagA- Hp infection (33.3%, P = 0.159). The positive Cx32 and Cx43 expression rates of the CSG patients with CagA+ Hp and CagA- Hp infection were all 100%, but the expression intensity of the CagA+ Hp group was significantly lower than that of the CagA- Hp group (P = 0.032). The positive Cx32 and Cx43 expression rates after Hp eradication of the precancerous lesion patients with Hp infection were 97.9% and 91.7% respectively, both significantly higher than those before eradication therapy (41.4% and 44.8% respectively, both P < 0.05). However, the positive Cx32 and Cx43 expression rates of the precancerous lesion patients with Hp infection without Hp eradication were still 40% and 50%, not significantly different from those before treatment.


CONCLUSIONS
The expression levels of Cx32 and Cx43 in gastric cancer and precancerous lesion decrease. The change of expression of Cx43 was associated with Hp infection, especially CagA+ Hp infection. Hp eradication in patients with precancerous lesion up-regulates the expression of Cx32 and Cx43.
Xu
Can-Xia
CX
Department of Gastroenterology, Third Xiangya Hospital, Central South University, Changsha 410013, China.
Jia
Yan
Y
Yang
Wen-Bin
WB
Wang
Fen
F
Shen
Shou-Rong
SR
D000328:Adult; D000368:Aged; D018031:Connexin 43 / Q000096:biosynthesis*; D017630:Connexins / Q000096:biosynthesis*; D005260:Female; D005756:Gastritis / Q000378:metabolism / Q000382:microbiology; D016481:Helicobacter Infections / Q000378:metabolism* / Q000382:microbiology; D016480:Helicobacter pylori; D006801:Humans; D007150:Immunohistochemistry; D008297:Male; D008875:Middle Aged; D011230:Precancerous Conditions / Q000378:metabolism* / Q000382:microbiology; D011446:Prospective Studies; D013274:Stomach Neoplasms / Q000378:metabolism* / Q000382:microbiology; D000097002:Gap Junction beta-1 Protein
D018031:Connexin 43; D017630:Connexins; D000097002:Gap Junction beta-1 Protein